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. Author manuscript; available in PMC: 2018 May 1.
Published in final edited form as: Pharmacol Ther. 2017 Jan 27;173:19–33. doi: 10.1016/j.pharmthera.2017.01.004

Fig. 1.

Fig. 1

Impact of CRBP1 and 2 on retinal reduction and RE biosynthesis. a) Model of CRBP2 actions in the intestinal enterocyte that direct retinoids into RE formation and arrests atRA biosynthesis. A brush border REH converts dietary vitamin A esters into retinol for absorption (Rigtrup & Ong, 1992; Rigtrup et al., 1994a; Rigtrup et al., 1994b). Alternatively, metabolism of carotenoids produces retinal. CRBP2 directs retinoids into RE formation and prevents atRA biosynthesis (Kakkad & Ong, 1988). b) Michaelis-Menten relationships of CRBP2-mediated retinal reduction and retinol esterification (Ong et al., 1987; MacDonald & Ong, 1988b). c) Kinetic constants demonstrating holo-CRBP2 channeling retinol through protein-protein interactions into RE biosynthesis. d) Model showing CRBP1 and 2 actions in liver directing retinol to LRAT for RE formation (Ong et al., 1988; MacDonald & Ong, 1988a; Yost et al., 1988; Randolph et al., 1991; Herr & Ong, 1992). e) Kinetic constants that illustrate ability of holo-CRBP1 to deliver retinol through protein-protein interaction to LRAT for RE biosynthesis in liver.